Oxidative stress induced change of Ubiquitin modification in Mineralocorticoid receptor and cardiovascular disorder
Project/Area Number |
20790664
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Endocrinology
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Research Institution | The University of Tokyo |
Principal Investigator |
YOKOTA Kenichi The University of Tokyo, 分子細胞生物学研究所, 特任研究員 (50424156)
|
Project Period (FY) |
2008 – 2009
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | MR / アルドステロン / ユビキチン / 転写 / エピゲノム |
Research Abstract |
Mineralocorticoid receptor(MR) is ubiquitinated and then led to proteasome mediated degradation by its ligand, Aldosterone.It is possible that oxidative stress may modify MR ubiquitination and thus change MR mediated transcription.The E3 ligase that regulates MR degradation is possibly UBR2 and it may modify MR degradation under oxidative stress.
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Report
(3 results)
Research Products
(3 results)